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Sixty-two newborn Holstein-Friesian calves were used to study the role of colostrokinin, serum cortisol, and serum thyroxine in the absorption of maternal immunoglobulin. Calves were removed from their dams prior to suckling and assigned one of four rations: colostrum, whole milk, milk plus colostral immunoglobulin, and milk plus immunoglobulin plus colostrokinin. Calves were fed their assigned ration either at birth or after twelve hours inanition. All calves were fed pooled colostrum at 24 hours postpartum. Blood samples were collected at seventeen times during the first 32 hours postpartum. Calves were born with high cortisol concentrations (88 ng/ml) which decreased (P < .05) within two hours postfeeding. Serum cortisol levels increased (P < .05) between two and three hours after calves ingested a colostral source of immunoglobulin. Time of initial feeding had no effect on the cortisol surge. No such increase was observed in neonates consuming an immunoglobulin-free milk ration. These results demonstrate that the immunoglobulin fraction of colostrum is responsible for initiating an increase in cortisol secretion by the adrenal cortex. Within four hours postpartum, serum thyroxine concentrations increased (P < .05) at least 50% in all treatment groups regardless of whether the calves were fed or fasted. After peaking at 18 μg/dL, the serum thyroxine concentrations fell gradually throughout the duration of the collection period. Colostrokinin exhibited a biphasic effect on serum immunoglobulin concentrations which was dependent on the initial time of feeding. Calves exposed to colostrokinin in 0 hour feedings had serum immunoglobulin G concentrations significantly higher (P < .05) after 16 hours postpartum than animals not fed colostrokinin. Fasted calves, exposed to colostrokinin at 12 hours postpartum, had no increase in serum immunoglobulin G concentrations following a colostrum feeding at 24 hours postpartum. Fasted calves fed a ration not containing colostrokinin exhibited a two-fold increase in serum immunoglobulin G concentrations after the 24 hour colostrum feeding. Colostrokinin did not have an immediate effect on serum immunoglobulin G concentrations, but required an approximate twelve hour period to manifest its regulatory function. The presence or absence of colostrokinin in the experimental rations did not have any effect on the cortisol or thyroxine profiles. The variable serum immunoglobulin G profiles suggest that colostrokinin is involved in the acquisition of passive immunity by the calf, but colostrokinin may have more than one physiological role.

In the second part of our study, cDNA of AQP-1 and pro-vasotocin were cloned from the silver sea bream. An AQP-1 full clone was isolated from kidney and intestine and it consists of 904 bp with an open reading frame of 774 bp. The deduced amino sequence of sea bream AQP-1 shares highest identity with AQP-1a of gilthead sea bream (97.7%) and AQP-1a of other fish species (83.6% to 95.8%), however, considerably low identity was found between the silver sea bream AQP-1 and AQP-1b of gilthead sea bream (56%). The silver sea bream AQP-1 possesses basic features of a functional aquaporin and AQP-1, which includes two channel-forming asparagine-proline-alanine (NPA) signature motifs, six transmembrane domains, residues of the pore-forming region and a potential mercurial inhibiting site (Cys-178). The water channel was ubiquitously expressed in gills, liver, intestine, rectum, kidney, heart, urinary bladder and blood cells. A partial fragment of pro-vasotocin was isolated from hypothalamus of silver sea bream and consists of 184 bp, including encoding regions for the processing and amidation signal, vasotocin hormone and part of the neurophysin. / Lastly, single doses of cortisol (50 microg/g tissue) or vasotocin (1 microg/g tissue) were administered to seawater-acclimated sea bream with further three-day stabilizing period in seawater followed by an abrupt 6&permil; exposure or administered to seawater transfer controls for three days. Cortisol markedly stimulated intestinal expression of AQP-1 in both the seawater transfer control and abrupt 6&permil; transfer groups. Vasotocin treatment did not significantly modify AQP-1 expression in all tested organs. Hypothalamic pro-vasotocin expression levels were similar among different treatment groups. / Semi-quantitative RT-PCR analysis was used for studying the effect of salinity and hormones on expression of AQP-1 and pro-vasotocin. In the long-term salinity acclimation experiment, the sea bream were acclimated to six different salinity regimes (0&permil;, 6&permil;, 12&permil;, 33&permil;, 50&permil;, 70&permil;) for four weeks. The abundance of AQP-1 transcript was the highest in intestine of 70&permil;-acclimated fish among different salinity groups and there was also a statistically significant increase in 12&permil;-acclimated fish. Branchial AQP-1 expression was significantly upregulated in sea bream acclimated to freshwater. In contrast, the hypothalamic pro-vasotocin expression was significantly downregulated during freshwater acclimation. In addition, the sea bream were also subjected to an abrupt 6%o transfer at different time intervals (2, 6, 12, 72 and 168 hours). RT-PCR analysis revealed there was a transient decrease in branchial AQP-1 expression two hours after abrupt hypo-osmotic exposure and the expression levels subsequently returned to the seawater control levels. The expression levels of hypothalamic pro-vasotocin were not significantly altered by the abrupt exposure treatment. / The present experiments investigated the effects of salinity and hormones on the relative expression of hypothalamic pro-vasotocin, and aquaporin-1 (AQP-1) in intestine, gills and kidney of the silver sea bream Sparus sarba. With the use of immunohistochemical techniques, immunoreactivity of AQP-1 was detected at the basal side of enterocytes and gill chloride cells, and at the apical brush border of kidney tubules whereas AQP-3 was only localized in similar positions in the gills and intestines. AQP-1 was relatively more ubiquitous than AQP-3 and was localized with same cell types as the electrogenic Na+-K+-ATPase in gills and kidney. / The present study had demonstrated the responsiveness of intestinal and branchial AQP-1 expressions of the silver sea bream to environmental salinity perturbations. Further to this, cortisol was observed to upregulate the transcription of AQP-1 in the intestine. Pro-vasotocin expression was altered by long-term salinity adaptation, however, the linkage of this alteration to AQP-1 functioning in different osmoregulatory organs is yet to be elucidated. / Luk, Chun Yin. / Adviser: Norman Y. S. Woo. / Source: Dissertation Abstracts International, Volume: 72-04, Section: B, page: . / Thesis (Ph.D.)--Chinese University of Hong Kong, 2010. / Includes bibliographical references (leaves 200-222). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. Ann Arbor, MI : ProQuest Information and Learning Company, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese.

[Truncated abstract] Obesity is rapidly increasing in prevalence and has significant physical and mental health implications. Stress, a general term referring to factors indicative of psychological strain such as depression and anxiety, has been identified as both a cause and consequence of weight gain and obesity in some individuals. In previous research, overeating in response to stress has been investigated as either a means of mood regulation or as a response to strict dietary restraint. Cortisol, a steroid hormone that increases in response to stress, has also been linked with increased food intake in both animal and human studies. Thus, cortisol may be an additional factor contributing to overeating and weight gain in response to stress. If stress does lead to overeating and weight gain, it is also likely that stress will inhibit attempts made by obese individuals at weight loss. The first study of this thesis was a repeated measures treatment study in which the associations of stress and cortisol levels with baseline body mass index and subsequent weight loss were investigated among females participating in a cognitive behavioural weight management programme. A cross-sectional analysis prior to treatment commencement showed that the association of stress and depression with body mass index was moderated by the severity of obesity. Dichotomous thinking, a cognitive style in which events are viewed in polarised 'black and white' terms, mediated the associations of both depression and eating disorder symptomatology with BMI. ... The second study of this thesis was a controlled laboratory-based examination of food intake following an acute psychological stressor. It was hypothesised that high baseline levels of psychological stress, such as depression and anxiety, would be associated with greater increases in negative mood and cortisol levels in response to the acute stressor, both of which, in turn, would be associated with greater food intake. Contrary to the hypothesis, baseline levels of psychological stress were not associated with the extent to which negative mood and cortisol levels increased following the acute stressor. The extent to which negative mood, but not cortisol, increased following acute stress was significantly positively associated with food intake. The results do not support the hypothesis that high cortisol levels are predictive of increased food intake in human females, although the results may have been affected by the broad participant inclusion criteria. The results suggest that increases in negative mood lead to increases in food intake, although it is argued that this is unlikely to be a general effect and suggestions for future research are made. The overall aim of this research was to examine whether stress and cortisol were associated with weight status, acute changes in eating behaviour and changes in weight in the medium-term. The results are discussed in relation to this aim, wth particular focus on the differences between treatment-seeking and community samples, implications for the treatment of obesity (especially when the individual is also experiencing high levels of depression), prevention of weight gain and possible future studies of the effects of stress and depression on weight change and eating behaviour.

Call number: LD2668 .T4 1985 P34 / Master of Science

Wild populations of fish are faced with a multitude of stressors, which may include human interaction, toxins, and disease. Benzo(a)pyrene (BaP), a known carcinogen and immunotoxin, has been reported in the stomach contents of juvenile chinook salmon, Oncorhynchus tshawytscha, in urban waterways. We investigated the impact of chronic dietary exposure of environmentally relevant levels of BaP on the immune system and cytochrome P4501A1 (CYP1A1) expression in juvenile chinook salmon. Two experiments were carried out in which juvenile fish were fed food treated with ethanol (control diet), low or high concentrations of BaP, or cortisol. In the first experiment we measured mitogen-stimulated proliferation of splenic leukocytes using flow cytometry and a colorimetric assay using Alamar Blue[superscript TM] Susceptibility to a microsporidian parasite, Loma salmonae, was evaluated in the second experiment by quantification of xenomas in the gills. Hepatic CYP1A1 and plasma cortisol were measured in both experiments. No significant trends were found in leukocyte mitogen activation or plasma cortisol between treatments or days. However, western blot analysis of CYP1A1 concentration in liver revealed interesting patterns of induction: in cortisol fed groups CYP1A1 was <20% of control on all days, groups fed low levels of BaP were 250% of control values on days 8 and 21 then dropped below control values on day 29, and groups fed high levels of BaP had less CYP1A1 than controls on all days. Similar patterns of CYP1A1 levels were found in the second experiment, and diseased control groups showed about a 55% decrease in CYP1A1 concentration when compared with non-diseased control groups. Susceptibility to L. salmonae was significantly higher in groups receiving cortisol. Whereas there was no effect of the high BaP dose, the low BaP dose appeared to increase disease susceptibility. This study supports concerns of stress and toxin induced immune dysfunction in wild populations of fish. / Graduation date: 2004

Abstract not available